Abstract
The aggressiveness of clear cell renal cell carcinoma (KIRC) plays a crucial role in patient prognosis. This study investigated the role of COL1A1 in KIRC progression and its underlying molecular mechanisms through bioinformatics analysis, in vitro experiments, and xenograft mouse models. COL1A1 expression was significantly upregulated in KIRC and correlated with poor patient outcomes. Knockdown of COL1A1 inhibited tumor cell proliferation, migration, and invasion in both in vitro and xenograft models, as well as suppression of epithelial-mesenchymal transition (EMT). Knockdown of COL1A1 also significantly reduced the protein levels of the stemness markers OCT4 and SOX2 in KIRC cells. Additionally, COL1A1 inhibition impaired activation of the PI3K/Akt signaling pathway. These findings underscore the pivotal role of the COL1A1/PI3K/Akt axis in KIRC progression and suggest potential therapeutic strategies targeting this pathway.